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A Surprising Clue to Tourette Syndrome


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One wonders how this may be related to PANDAS given histamine is involved in the immune response?

 

http://news.sciencemag.org/sciencenow/2010...o-tourette.html

 

People with Tourette syndrome are plagued by unwanted movements and verbal tics that run the gamut from extra eye blinks and grimaces to involuntary grunts or even cursing. Although the disorder tends to run in families, little is known about its genetic basis. Now researchers have found a mutated gene that appears to cause the disorder in one extremely unusual family with nine afflicted individuals. Although this mutation is not the cause of the vast majority of Tourette syndrome cases, it may push researchers to investigate a mechanism—and potential treatments—they otherwise would not have considered.

 

Since the French neurologist Georges Gilles de la Tourette first described his namesake condition 125 years ago, scientists have puzzled over the cause. Much recent attention has focused on a brain region called the basal ganglia that is involved in repetitive behaviors and on the neurotransmitter dopamine. In 2005, a team led by child psychiatrist and geneticist Matthew State of Yale University School of Medicine, reported one of the first genetic clues to the disorder, a mutation in a gene called SLITRK1 that seems to be responsible for a rare handful of cases. But the function of SLITRK1 and its contribution to Tourette syndrome are still largely a mystery.

 

In the new study, State and colleagues examined a family in which the father and all eight offspring (six sons and two daughters) have the syndrome. Extensive genetic detective work led them to a mutation in a gene called HDC, which encodes L-histidine decarboxylase, an enzyme involved in the production of histamine, a signaling molecule with a wide variety of roles throughout the body. The same mutation was present in all members of the family who had Tourette but was absent in thousands of DNA samples from control subjects, who included unrelated people with similar ethnic backgrounds as well as a group of 720 Tourette patients, the researchers report today in The New England Journal of Medicine. The mutated version of the HDC gene likely results in a truncated version of the enzyme, which would result in reduced histamine levels, State says.

 

More info at the link above.

 

I posted recently that vitamin C may be helping my dd. The following link may explain why.

 

Some info on histamine from digital natropath: http://www.digitalnaturopath.com/cond/C376401.html

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The same mutation was present in all members of the family who had Tourette but was absent in thousands of DNA samples from control subjects, who included unrelated people with similar ethnic backgrounds as well as a group of 720 Tourette patients, the researchers report today in The New England Journal of Medicine. The mutated version of the HDC gene likely results in a truncated version of the enzyme, which would result in reduced histamine levels, State says.

 

if I am reading that correctly, this mutation was familial and the other TS patients did *not* have it???? so I am not seeing the "clue to Tourette Syndrome" there???? unless I am missing something?

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it is an interesting study but makes me wonder tho on how widespread this could be?

 

I know of a number of TS patients who actually take benedryl (anti-histamine) for allergies and feel it helps reduce their tics, as well as so many TS people who seem to also have the seasonal allergies, that usually indicate high histamine, yes?

 

I am a biochemistry dummy (as Kim can verify :blink: ) so maybe I am not understanding?

Edited by Chemar
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I would agree with Chemar on this one.....but maybe they are saying it may indicate a histamine sensitivity setting people off...which is kind of what this board is all about...what sets people off.....

like why alot of us seem to have exasperation during different pollen seasons or reactions to food and milk...

.DID i even make sense?...if not ignore....its just a big circle of different sensitivieites for everyone.....

 

The same mutation was present in all members of the family who had Tourette but was absent in thousands of DNA samples from control subjects, who included unrelated people with similar ethnic backgrounds as well as a group of 720 Tourette patients, the researchers report today in The New England Journal of Medicine. The mutated version of the HDC gene likely results in a truncated version of the enzyme, which would result in reduced histamine levels, State says.

 

if I am reading that correctly, this mutation was familial and the other TS patients did *not* have it???? so I am not seeing the "clue to Tourette Syndrome" there???? unless I am missing something?

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The last paragraph from the article gives a bit more info:

 

"If histamine is actually an active player in Tourette's syndrome, it really would open up a whole new avenue of treatment" involving drugs that boost histamine, says Jeremiah Scharf, a behavioral neurologist and neurogeneticist at Harvard Medical School in Boston. But he cautions that a lot more work is needed to determine if the findings from this one family can be put to use to help the thousands of other people with the disorder.

 

I did read something about histamine in the blood differing from levels in the brain? And according to this article antihistamine meds have a varied impact on the brain depending.

 

It may be a dead end, but I thought that histamines role in immune function was interesting in the context of PANDAS and so on. I'm still trying to research how strep may impact histamine in the brain to see if there is a potential connection. Anyone?

 

I realize this research may sound as if it's opposed to PANDAS, but I wonder if it may bolster the potential connection depending upon how blood and brain histamine react under various circumstances.

 

Sorry, just thinking out lout... :wacko:

 

Edited for spelling/grammar. sheesh!

Edited by Laurensmom
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More info on various types of histamine receptors.

 

https://www.neurorelief.com/newsletterarchive.php?issue=349

There are at least four types of histamine receptors (H1...H4) numbered according to their order of discovery.

 

H1

H1 receptors are located in the periphery in the smooth muscles of intestines, bronchi, and blood vessels, as well as the CNS and are the main target for the antihistamine medications used to address allergies and the immune response. H1 receptors within the central nervous system are also responsible for the stimulatory properties of histamine and the improvement in cognitive function, vigilance, and memory caused by histamine.

 

H2

H2 receptors on neurons are primarily post-synaptically located and receptors are coupled to adenylyl cyclase and increase cAMP for energy production. High densities of H2 receptors are found within the CNS. Activation of these receptors has primarily an excitatory effect on neurotransmission via alterations in ion channel activity that favor neuron depolarization.

 

The H2 receptors are also present in the periphery, including the gastric mucosa, immune cells, and myocytes. Drugs acting on the H2 receptors in the gut prevent histamine from stimulating the secretion of gastric acid and have been widely prescribed for the treatment of gastro-esophageal reflux and peptic ulcer disease.

 

In general, H2 receptor blockers do not cross the blood-brain barrier. Common examples are: Cimetidine (Tagamet), Ranitidine (Zantac), Famotidine (Pepcid), Nizatidine (Axid).

 

In patients with poor digestion increasing gastric acid production by increasing histamine can aid digestion by stimulating acid secretion.

 

H3

H3 are believed to be auto-receptors that act to down-regulate histamine release and synthesis and thereby reduce the effects of H1 and H2 receptors. However the greatest concentration of H3 receptors exist in areas of the brain that have more non-histamine neurons. As such, histamine release, acting via the H3 receptor, can modulate the activity of serotonin and dopamine neurons as well. Behavioral animal studies have shown that enhancing the actions of histamine, through the use of H3 receptor blockers, causes significant improvements in memory and learning.

 

H4

H4 receptors have only recently been discovered and seem in some ways to act like H3 receptors but are located in mast cells as well as in the CNS. They seem to increase calcium mobilization from intracellular calcium stores.

 

More from the NEJM. Hoping someone here can make some sense of this info. :wacko: I wonder if at times the body over compensates after a bacterial/viral assault and depletes H3 from the brain in the process?

 

Again, just thinking outloud and posting info for the record.

 

http://content.nejm.org/cgi/content/full/NEJMoa0907006

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Ah ha! I think I found something of interest ... this conversation may explain the paradox Chemar and I discussed above?

 

http://www.prohealth.com/fibromyalgia/blog...l.cfm?id=731019

 

I have posted about this several times...taking histidine literally gave me my life back. I still have to take it every day to keep down the allergic responses (food, pollen, chemicals, etc) but the amount I take varies according to my total load.

 

The two brands I prefer are Montiff and Jo-Mar. You can find both on the internet. If you take histidine you do need about 15-20mg zinc for every 500mg of histidine.

 

Eddie, while high histamine can be a problem, especially in certain types of mental illness, there's a paradoxical effect in that the higher your blood levels of histidine, the slower the mast cells are to release histamines. For the conversion to take place it also requires zinc and B6, so for that reason I suggest that people keep their zinc levels adequate, but not high and avoid the histidine supplements that include B6 unless they are trying to use it to increase histamines (this is another topic, but it affects sexual function).

 

I have been using histidine for about 15 years now and even wrote a paper on it for my sports nutrition certification. It's an amazingly overlooked amino acid...many of my clients with IBS improved dramatically, too, since it decreases cytokine production in the intestines and increases calcium absorption which slows smooth muscle contraction.

 

Perhaps this explains why antihistamines have been helpful to some with PANDAS?

 

GREAT info at nutripedia > http://www.nutripedia.com/Amino_Acids/L-Histidine.html

 

There are some natural health practitioners who have used L-histamine for ADHD etc. Seems they may have been ahead of the "science?" :)

 

http://www.add-adhd-help-center.com/Ingred.../lhistidine.htm ( A helpful food list at the link as well).

 

Histidine Food Sources

 

Bananas and grapes, meat and poultry, and milk and milk products are high in Histidine. It is also found in root vegetables, wheat, rice and all green vegetables, though in lesser quantities.

 

Sorry gang, I'm excited about the potential this research merits and wanted to create an information dump (if you will) as I do more digging. Thanks for your patience with me. :D

Edited by Laurensmom
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This is a good one....i 'm tired and not as sharp on the science sturff as others but there a couple of threads and stephanie2 and someone else talks about pecid a/c and something (aslo per scott smith) being histamine blockers...

i hope that was coherent...

very tired...

 

 

More info on various types of histamine receptors.

 

https://www.neurorelief.com/newsletterarchive.php?issue=349

There are at least four types of histamine receptors (H1...H4) numbered according to their order of discovery.

 

H1

H1 receptors are located in the periphery in the smooth muscles of intestines, bronchi, and blood vessels, as well as the CNS and are the main target for the antihistamine medications used to address allergies and the immune response. H1 receptors within the central nervous system are also responsible for the stimulatory properties of histamine and the improvement in cognitive function, vigilance, and memory caused by histamine.

 

H2

H2 receptors on neurons are primarily post-synaptically located and receptors are coupled to adenylyl cyclase and increase cAMP for energy production. High densities of H2 receptors are found within the CNS. Activation of these receptors has primarily an excitatory effect on neurotransmission via alterations in ion channel activity that favor neuron depolarization.

 

The H2 receptors are also present in the periphery, including the gastric mucosa, immune cells, and myocytes. Drugs acting on the H2 receptors in the gut prevent histamine from stimulating the secretion of gastric acid and have been widely prescribed for the treatment of gastro-esophageal reflux and peptic ulcer disease.

 

In general, H2 receptor blockers do not cross the blood-brain barrier. Common examples are: Cimetidine (Tagamet), Ranitidine (Zantac), Famotidine (Pepcid), Nizatidine (Axid).

 

In patients with poor digestion increasing gastric acid production by increasing histamine can aid digestion by stimulating acid secretion.

 

H3

H3 are believed to be auto-receptors that act to down-regulate histamine release and synthesis and thereby reduce the effects of H1 and H2 receptors. However the greatest concentration of H3 receptors exist in areas of the brain that have more non-histamine neurons. As such, histamine release, acting via the H3 receptor, can modulate the activity of serotonin and dopamine neurons as well. Behavioral animal studies have shown that enhancing the actions of histamine, through the use of H3 receptor blockers, causes significant improvements in memory and learning.

 

H4

H4 receptors have only recently been discovered and seem in some ways to act like H3 receptors but are located in mast cells as well as in the CNS. They seem to increase calcium mobilization from intracellular calcium stores.

 

More from the NEJM. Hoping someone here can make some sense of this info. :) I wonder if at times the body over compensates after a bacterial/viral assault and depletes H3 from the brain in the process?

 

Again, just thinking outloud and posting info for the record.

 

http://content.nejm.org/cgi/content/full/NEJMoa0907006

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Well, antihistamine send my child into a wild rage, so it could be something relevant to her condition. She also has almost no IgE- which activates mast cells to release histamine. I'll be revisiting these studies when I have more time. Thanks!

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